SLC39A14 and hereditary hemochromatosis: In a murine model of hereditary hemochromatosis, SLC39A14 was found essential in promoting hepatocellular iron overload.[31] In addition, SLC39A14 could mediate NTBI uptake and cause intestinal injury and intestinal flora dysbiosis.[32] Of note, in the present study, knockdown of SLC39A14 in AOLT rats significantly reversed the increased iron content in liver, while the serum iron level was notably higher compared to SLC39A14‐NC AOLT rats.